In physics, work is the product of a force and a distance. Therefore, considering a solid object of a given mass, the work done to move the object is the force applied to the object times the distance that the object moves. In the case of the work done to move a volume of fluid, work is defined as the product of the volume of fluid and the pressure required to move the fluid. Stroke work (SW) refers to the work done by the ventricle to eject a volume of blood (i.e., stroke volume) into the aorta. The force that is applied to the volume of blood is the intraventricular pressure.
The interplay between ventricular function (including both ventricular filling and ejection) and the circulation can be seen when ventricular pressure is plotted against ventricular pressure at various points in time. FIG. 1 illustrates a pressure volume loop 100 as known in the art. The pressure volume loop 100 reflects the cardiac cycle of ventricular filling (a), isovolumetric contraction (b), ventricular ejection (c) and isovolumetric relaxation (d).
The end-diastolic volume (EDV) 130 is the maximum volume achieved at the end of filling, and end-systolic volume (ESV) 140 is the minimal volume (i.e., residual volume) of the ventricle found at the end of ejection. The width of the loop, therefore, represents the difference between EDV and ESV, which is by definition the stroke volume 110 (SV). The cardiac cycle, and the work performed by the heart, is confined within boundaries that define this interaction at end-diastole (the end-diastolic pressure-volume relationship or EDPVR 120) and at end-systole (the end-systolic pressure volume relationship or ESPVR 115). The ESPVR 115 is the maximum pressure at any given left ventricular volume that can be developed by the ventricle and represents the inotropic state of the ventricle. The slope of the ESPVR 115 is independent of ventricular loading and is a measure of the inherent contractility of the ventricle at that time.
The area of the pressure-volume loop 110 represents stroke work, which is the work of the heart each heart beat. While prior art pacing devices are focused on increasing cardiac output, the long term health of the cardiac patient would be improved by techniques that reduce the work required to eject a given volume of blood during a heart beat thereby increasing cardiac efficiency.
Ischemia is an oxygen starvation of the myocardium that is a precursor to myocardial infarction or the death of the starved myocardial cells. Angina pectoris is chest pain brought on by ischemic myocardial tissue. The pain comes approximately when the demand of the heart muscle for oxygen exceeds the ability of the coronary arteries to deliver it. The amount of oxygen extracted by the heart muscle in order to produce useful heart muscle contraction is related to the amount of work the heart muscle has to do, and more especially on the pressure against which the heart has to pump the blood. Thus, on exercise, more work is done and more oxygen required. Heart rate and blood pressure typically rise to try to help supply the need. If the myocardium is made more efficient, i.e. able to develop the needed hemodynamics with less work, the threshold for development of chest pain will be raised, and the patient will be better able to exercise.
It would be useful to provide a method of reducing ischemia by reducing the stroke work of the ventricles.